Non-fucosylated Anti-Human TNF (Infliximab) Therapeutic Antibody (CAT#: BioBet-021ZP) Datasheet

TNF

tumor necrosis factor

This gene encodes a multifunctional proinflammatory cytokine that belongs to the tumor necrosis factor (TNF) superfamily. This cytokine is mainly secreted by macrophages. It can bind to, and thus functions through its receptors TNFRSF1A/TNFR1 and TNFRSF1B/TNFBR. This cytokine is involved in the regulation of a wide spectrum of biological processes including cell proliferation, differentiation, apoptosis, lipid metabolism, and coagulation. This cytokine has been implicated in a variety of diseases, including autoimmune diseases, insulin resistance, and cancer. Knockout studies in mice also suggested the neuroprotective function of this cytokine.

DIF; TNFA; TNFSF2; TNLG1F; TNF-alpha

Plasma membrane, Extracellular region or secreted

Diseases associated with TNF include Asthma and Malaria.

Its related pathways are Apoptosis Modulation and Signaling and Monoamine Transport.

1.Cytokines that bind to TNFRSF1A/TNFR1 and TNFRSF1B/TNFBR. It is mainly secreted by macrophages and can cause cell death in certain tumor cell lines. It is a strong pyrogen that directly acts or stimulates the secretion of interleukin-1 to cause fever. It is related to the induction of cachexia and can stimulate cell proliferation and induce cell differentiation under certain conditions. Dephosphorylation of FOXP3 impairs the function of regulatory T cells (Treg) in rheumatoid arthritis individuals. Up-regulating the expression of protein phosphatase 1 (PP1), PP1 dephosphorylates the key Ser-418 residue of FOXP3, thereby inactivating FOXP3 and deficient in Treg cell function (PubMed:23396208). In the RT4v6 bladder cancer cell line, bcg-stimulated neutrophils combined with DIABLO/SMAC mimics are key mediators of cell death in the anticancer effect (PubMed:22517918, PubMed:16829952, PubMed:23396208). By inhibiting insulin-induced IRS1 tyrosine phosphorylation and insulin-induced glucose uptake, it induces insulin resistance in adipocytes. Induces the degradation of GKAP42 protein in adipocytes, which is partly involved in tnf-induced insulin resistance (similar). 2. The formation of TNF intracellular domain (ICD) can induce dendritic cells to produce IL12.

Cancer antibody; Cell Biology and Cellular Response antibody; Immune System antibody; Metabolism antibody; Signaling Transduction antibody

1.The soluble form derives from the membrane form by proteolytic processing. The membrane-bound form is further proteolytically processed by SPPL2A or SPPL2B through regulated intramembrane proteolysis producing TNF intracellular domains (ICD1 and ICD2) released in the cytosol and TNF C-domain 1 and C-domain 2 secreted into the extracellular space. 2.The membrane form, but not the soluble form, is phosphorylated on serine residues. Dephosphorylation of the membrane form occurs by binding to soluble TNFRSF1A/TNFR1. 3.O-glycosylated; glycans contain galactose, N-acetylgalactosamine and N-acetylneuraminic acid.

Protein Based Therapies
Monoclonal antibody (mAb)

IgG1

Infliximab

Mouse

Human

Infliximab is a monoclonal IgG1 antibody that specifically targets tumor necrosis factor (TNF-α or TNF-α). Infliximab was used for the treatment of various inflammatory diseases, such as chronic Crohn's disease in adults or children, ulcerative colitis in adults or children, rheumatoid arthritis and methotrexate , Ankylosing spondylitis, psoriatic arthritis, and plaque psoriasis.

Ankylosing Spondylitis (AS)
Crohn's Disease (CD)
Psoriasis Vulgaris (Plaque Psoriasis)
Psoriatic Arthritis
Rheumatoid Arthritis
Ulcerative Colitis

infliximab-axxq, infliximab-qbtx, infliximab-abda, infliximab-dyyb

Infliximab is a chimeric gG1κ monoclonal antibody that binds to soluble and transmembrane forms of TNF-α with high affinity, thereby blocking proinflammatory cascade signaling. Binding of the antibody to TNF-α prevents TNF-α from interacting with its receptor. Tumor necrosis factor-α (TNF-α) is a key pro-inflammatory cytokine involved in chronic inflammatory diseases. Its excessive activity and enhanced signaling pathways can be observed in inflammatory diseases and activate further pro-inflammatory cascades. By mediating ADCC and CDC effects, infliximab may also lead to lysis of TNF-α1 producing cells.

Ankylosing Spondylitis (AS)
Crohn's Disease (CD)
Psoriasis Vulgaris (Plaque Psoriasis)
Psoriatic Arthritis
Rheumatoid Arthritis
Ulcerative Colitis